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志贺毒素 2 在与严重人类疾病相关的大肠杆菌 O157:H7 菌株中的过度表达。

Shiga toxin 2 overexpression in Escherichia coli O157:H7 strains associated with severe human disease.

机构信息

Microbial Evolution and Epidemiology Laboratory, Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, United States.

出版信息

Microb Pathog. 2011 Dec;51(6):466-70. doi: 10.1016/j.micpath.2011.07.009. Epub 2011 Aug 16.

DOI:10.1016/j.micpath.2011.07.009
PMID:21864671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3205445/
Abstract

Variation in disease severity among Escherichia coli O157:H7 infections may result from differential expression of Shiga toxin 2 (Stx2). Eleven strains belonging to four prominent phylogenetic clades, including clade 8 strains representative of the 2006 U.S. spinach outbreak, were examined for stx2 expression by real-time PCR and western blot analysis. Clade 8 strains were shown to overexpress stx2 basally, and following induction with ciprofloxacin when compared to strains from clades 1-3. Differences in stx2 expression generally correlated with Stx2 protein levels. Single-nucleotide polymorphisms identified in regions upstream of stx2AB in clade 8 strains were largely absent in non-clade 8 strains. This study concludes that stx2 overexpression is common to strains from clade 8 associated with hemolytic uremic syndrome, and describes SNPs which may affect stx2 expression and which could be useful in the genetic differentiation of highly-virulent strains.

摘要

大肠杆菌 O157:H7 感染的疾病严重程度的差异可能是由于志贺毒素 2(Stx2)的差异表达所致。通过实时 PCR 和 Western blot 分析,对属于四个主要系统发育分支的 11 株菌(包括代表 2006 年美国菠菜暴发的 8 型分支菌株)进行了 Stx2 表达检测。与 1-3 型分支的菌株相比,8 型分支的菌株在基础水平上过度表达 Stx2,并且在用环丙沙星诱导后也是如此。Stx2 表达的差异通常与 Stx2 蛋白水平相关。在 8 型分支菌株 stx2AB 上游区域中鉴定的单核苷酸多态性在非 8 型分支菌株中基本上不存在。本研究得出的结论是,与溶血性尿毒综合征相关的 8 型分支菌株普遍存在 Stx2 过度表达,并描述了可能影响 Stx2 表达的 SNPs,这些 SNPs 可能有助于高度毒力菌株的遗传分化。

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Quantifying E. coli proteome and transcriptome with single-molecule sensitivity in single cells.在单细胞中实现单分子灵敏度定量大肠杆菌的蛋白质组和转录组。
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The CI repressors of Shiga toxin-converting prophages are involved in coinfection of Escherichia coli strains, which causes a down regulation in the production of Shiga toxin 2.志贺毒素转换前噬菌体的CI阻遏物参与大肠杆菌菌株的共感染,这会导致志贺毒素2的产生下调。
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